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CPR > Test 4 > Flashcards

Test 4 Flashcards

1
Q

What is PACO2? PAO2?

A

Alveolar partial pressure of CO2

Alveolar partial pressure of O2

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2
Q

What is PaO2? PaCO2?

A

Arterial partial pressure of O2

Arterial partial pressure of CO2

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3
Q

What is PcO2? PcCO2?

A

Pulmonary capillary partial pressure of O2

Pulmonary capillary partial pressure of CO2

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4
Q

What is VE? (V with dot above it)

A

Volume expired per minute

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5
Q

What is FIO2?

A

Inspired fraction of oxygen

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6
Q

What is PvO2?

A

Venous partial pressure of O2

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7
Q

What is the equation for partial pressure?

A

PGas = PTotal x F

PTotal = total pressure

F = fractional concentration (e.g. 21%)

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8
Q

What is the oxygen transport cascade?

A

the change in partial pressure of oxygen as is moves from the environment, through the lungs, into the blood, out to the tissues, and back to the heart in the venous circulation

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9
Q

What is the PO2 in ambient air? Inspired air? Alveolar space? Pulmonary capillary? Arterial blood? Tissue capillaries? Venous Blood?

A
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10
Q

What is barometric pressure? How does it change with altitude?

A

atmospheric pressure

It decreases as altitude increases

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11
Q

What is barometric pressure at sea level?

A

1 atm = 760 torr = 760 mmHg

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12
Q

What is the percentage of O2 in the air?

A

21%

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13
Q

If O2 percentage is 21%, what is the PO2 at sea level?

A

PO2 = 760 mmHg x .21

PO2 = 160 mmHg

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14
Q

What is inspired air?

A

As air enters the conducting airways of the respiratory tract it is rapidly warmed to body temperature and becomes fully saturated with water vapor, forming a gas mixture referred to as inspired air

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15
Q

At a normal body temperature of 37°C, what is the water vapor pressure of inspired air?

A

47 mmHg

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16
Q

What is the partial pressure of oxygen in inspired air in the upper airways (PIO2) at sea level?

A

PIO2 = (PB – 47 mmHg) X FIO2

PIO2 = (760mmHg – 47 mmHg) X .21

PIO2 = 150 mmHg

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17
Q

What factors determine the partial pressure of O2 in the alveolus (PAO2)?

A

1) PIO2 and minute ventilation (VA)
2) Cardiac output and tissue O2 consumption

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18
Q

What is the Alveolar Gas Equation?

A

PAO2 = (PB – PH2O) x FIO2 – (PaCO2/R)

PB = barometric pressure

PH2O = vapor pressure

FIO2 = fraction of inspired O2 (21%)

PaCO2 = Partial pressure of arterial CO2

R = Respiratory exchange ratio (0.8)

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19
Q

What is the respiratory exchange ratio?

A

0.8

Represents the volume of CO2 eliminated and the net volume of O2 taken up by the lungs

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20
Q

What 5 factors determine the rate of diffusion?

A

The partial pressure gradient between the alveolus and the capillary blood
The molecular weight of the diffusing molecule
The length of the diffusion pathway (in the lungs, this pathway is very short)

The total capillary surface area available for diffusion

The solubility of the molecule

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21
Q

What is the capillary transit time of a RBC in the lungs? How much time is needed to make

PcO2 = PAO2? How does a thickened alveolar capillary bed affect the time to make PcO2 = PAO2?

A

.75 seconds

.25 seconds or less

it increases the time (see the attached picture)

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22
Q

Once oxygen diffuses into the pulmonary capillary, in what two forms is it carried in the blood?

A

1) Hemoglobin
2) Physical solution

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23
Q

How is the concentration of a gas in physical solution calculated?

A

C = α x P

C = concentration

α = solubility

P = partial pressure

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24
Q

How does the solubility of a gas change with temperature?

A

As temperature increases, the solubility of a gas decreases

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25
Q

How is hemoglobin saturation calculated?

A

% saturation = (Actual Hb-O2 Content ÷ Total Hb-O2 Capacity) x 100

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26
Q

What is the percent saturation of hemoglobin at PO2 27 mmHg? PO2 40 mmHg? PO2 100 mmHg?

A

50%

75%

97.5%

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27
Q

How does pH, PCO2, Temperature, and 2,3-DPG affect Hb’s affinity for O2?

A

decrease in pH = decreased affinity

increase of PCO2 = decreased affinity

increase in temperature = decreased affinity

increase in 2,3-DPG = decreased affinity

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28
Q

How is total O2 content calculated?

A

O2 Content = ([Hb] x 1.39 x SO2) + (0.003 x PO2)

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29
Q

What does is this graph showing us?

A

The amount of O2 in physical solution and bound to hemaglobin and the total O2 content on a Hb-)2 dissociation curve

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30
Q

Could we survive by only distributing O2 to tissues in physical solution?

A

Nope! We rely heavily on hemoglobin

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31
Q

What happens to Hb saturation when the amount of Hb decreases? What happens to O2 content when the amount of Hb decreases?

A

% saturation will NOT change

The O2 content will derease (see graph and NOTE the difference in Y-axis)

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32
Q

What is the Alveolar-Arterial Oxygen Difference ([A-a]∆O2)?

A

[A-a]∆O2 is the difference of partial pressures between the alveolis and the arterial. The arterial partial pressure is ALWAYS lower than the alveolus due to “shunting”. This means that some of the circulating blood passes from the systemic venous to the systemic arterial circulation without meeting the gas exchange surface of the lung.

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33
Q

How is delivery of O2 to the tissues calculated?

A

DO2 = Cardiac output (Q) x CaO2

Remember:

CaO2 = ([Hb] x 1.39 x SO2) + (0.003 x PO2)

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34
Q

What does this represent? How is is calculated?

A

O2 consumption

The amount of O2 consumed by the tissues

Fick equation:

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35
Q

How does low PaO2 affect ventilation? What is the response called?

A

it triggers an increase in minute ventilation

(the amount of air, in liters, that a person breathes per minute.)

Hypoxic ventilatory response (HVP)

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36
Q

How does low PAO2 affect the pulmonary vasculature system? What is the response called?

A

A decrease in PAO2 results in vasocaonstriction to decrease blood flow to that area of the lung

hypoxic pulmonary vasoconstriction (HPV)

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37
Q

How does hypoxia affect the cardiovascular system?

A

Resting heart rate increases leading to an increase in cardiac output that helps maintain oxygen delivery to the tissues in the face of the diminished arterial oxygen content.

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38
Q

How does hypoxia affect the hematological system?

A

Decreased PaO2 causes an increase in serum erythropoietin (EPO) concentration.

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39
Q

How does hypoxia affect tissue-level responses?

A

Hypoxia results in the synthesis of hypoxia inducible factor 1-α (HIF-1α).

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40
Q

Name 2 dyshemoglobinemias

A

carboxyhemoglobinemia

methemoglobinemia

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41
Q

What is Carboxyhemoglobinemia? How does it affect Hb? Why is this bad?

A

high levels of CO in the blood

Hb has a much higher affinity for CO than O2. This means very little O2 will bind to Hb. In addition, high levels of CO result in an increased affinity for O2, which prevents the release of O2

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42
Q

What is methemoglobinemia? How does it affect Hb? Why is this bad?

A

In this disorder, the ferrous iron (2+ valence) in the heme moiety is oxidized to ferric iron (3+ valence)

This prevents O2 from binding to Hb

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43
Q

Would supplemental O2 help a patient with carboxyhemoglobinemia? Methemoglobinemia?

A

yes

no

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44
Q

What is cyanide poisoning? How does it work?

A

Cyanide poisoning decouples oxidative phosphorylation. More specifically, it binds to cytochrome c oxidase (complex IV).

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45
Q

How does cyanide poisoning, carboxyhemoglobinemia, and methemoglobinemia chnage PaO2, SpO2, and CvO2 and SvO2?

A
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46
Q

What does this indicate?

A

The amount of CO2 produced per minute

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47
Q

What are the ways CO2 is transported in the blood?

A

physical solution

Combination with a protein (Hb)

Bicarbonate

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48
Q

Draw a diagram showing the different ways CO2 is transported

A

Notice that conversion of CO2 + H2O –> H2CO3 is fast in the plasma. This is due to presence of carbonic anhydrase in the RBC cytoplasm. Another reason why conversion of CO2 + H2O –> H2CO3 is fast in the RBC is due to Hbs ability to bind protons, further moving the rxn to the right.

Also, notice how carbamino formation does not occur in the plasma. This is because Hb only resides in RBCs

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49
Q

What is this graph showing us?

A

1) The graph is showsing us the relationship between PO2 and PCO2. Between 40 mmHg and 46 mmHg, the CO2 content can drastically change. This change is further increased by increasing the PO2. The ability to unload CO2 with minimal change in PCO2 minimizes the change in pH between venous and arteriole blood
2) the total CO2 content in the body is MUCH higher than the O2 content

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50
Q

CO2 has a higher solubility compared to O2. Why then is the rate of CO2 transfer from the blood to the alveolar space almost identical to the diffusion of O2?

A

this is due to the time required to convert bicarbonate ion back to CO2 before diffusion can occur

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51
Q

How is minute ventilation calculated?

A

VT = Tidal volume

f = breathing frequency (respiratory rate)

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52
Q

What are the two components of minute ventilation?

A

dead space ventilation

alveolar ventilation

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53
Q

What is the anatomic dead space and alveolar dead space?

A

At the end of inspiration, the volume of air remaining in the conducting airways is the anatomic dead space (“dead” because it does not participate in gas exchange). In addition, any alveoli that are ventilated with air but not perfused with blood do not participate in gas exchange are therefore termed alveolar dead space.

54
Q

What is the physiologic dead space?

A

VD,Physiologic = VD,Anatomic + VD,Alveolar

55
Q

Describe how dead-space ventilation creates stale air and how it mixes with fresh air? (Use 500mL of inspired air as example)

A
56
Q

How is the dead space or wasted ventilation expressed?

A

as a fraction

57
Q

How would dead space or wasted ventilation change with exercise? increase in pulmonary flow? decrease in tidal volume?

A

exercise would increase tidal volume and would therefore decrease VD/VT

Increase in pulmonary flow would decrease the amount of alveolar dead spaces and would therefore decrease VD/VT

Decrease in tidal volume would increase VD/VT

58
Q

What is alveolar ventilation?

A

The portion of ventilation that participates in gas exchange because it contacts perfused alveoli

59
Q

How is alveolar ventilation calculated?

A

E = expired total ventilation

D,Physiologic = anatomic and alveolar dead spaces

f = respiratory rate

60
Q

Case 1: The Anxious Patient. Suppose an otherwise healthy man all of a sudden becomes very anxious. How will this affect is alveolar ventilation?

A

His physiologic dead space will not change, but his tidal volume and/or respiratory rate will increase. Therefore, his alveolar ventilation will increase.

61
Q

Case 2: Pulmonary Embolism. Suppose a woman develops a pulmonary embolism. As you will learn later in the course, this occurs when thrombus forms in a deep vein of the extremities and travels to the lung where it lodges in and obstructs the pulmonary arteries. Assuming her minute ventilation stays the same, how will this affect her alveolar ventilation?

A

The embolism will increase the amount of alveolar dead space, therefore increase the physiologic dead space. This will decrease alveolar ventilation

62
Q

What is the normal range for PaCO2?

A

35 - 45 mmHg

63
Q

What is hypercapnia? Hypocapnia?

A

Hypercapnea = PaCO2 > 45 mmHg

Hypocapnea = PaCO2 < 35 mmHg

64
Q

What is the relationship of PaCO2 with alveolar ventilation and the amount of CO2 produced?

A
65
Q

Case 1: The Anxious Patient. Suppose an otherwise healthy man all of a sudden becomes very anxious. How will this affect is alveolar ventilation? How will it affect PaCO2?

A

Alveolar ventilation will increase. An increase in alveolar ventilation will result in a decrease in arterial partial pressure of CO2

66
Q

Case 2: Pulmonary Embolism. Suppose a woman develops a pulmonary embolism. As you will learn later in the course, this occurs when thrombus forms in a deep vein of the extremities and travels to the lung where it lodges in and obstructs the pulmonary arteries. Assuming her minute ventilation stays the same, how will this affect her alveolar ventilation? How will this affect PaCO2?

A

physiological deadspace will increase resulting in a decrease in alveolar ventilation. A decrease in alveolar ventilation will result in an increase in arterial partial pressure of CO2

67
Q

What is hyperventilation?

A

ventilation in excess of metabolic needs. In other words, alveolar ventilation is higher than necessary for a given level of CO2 production.

68
Q

What is hypoventilation?

A

ventilation that is insufficient for metabolic needs. In other words, alveolar ventilation is lower than necessary for a given level of CO2 production.

69
Q

How does hyperventilation and hypoventilation affect PIO2? PaCO2? R? PAO2?

A
70
Q

What are the key features of hyperventilation and and hypoventilation?

A
71
Q

What is tidal breathing? Tidal volume?

A

This refers to normal breathing at rest. The volume inhaled with each breath is referred to as the tidal volume (VT).

72
Q

What is Functional Residual Capacity (FRC)?

A

This is the amount of air left in the lungs after the end of exhalation during tidal breathing.

73
Q

What is residual volume?

A

If an individual exhales to the fullest extent, the lungs do not completely empty. RV is the volume of air that remains in the lung at the end of a maximal exhalation.

74
Q

What is total lung capacity?

A

The volume of air in the lungs at the end of a maximal inhalation.

75
Q

How does air flow relate to pressure and resistance?

A

delta P is the difference between the pressure of outside air and the pressure within the alveolar space

76
Q

What is transmural pressure? How is it calculated?

A

The pressure differential across the wall of the structure is called the transmural pressure (PTM) and is determined by the pressure inside the structure (PIN) relative to the pressure outside the structure (POUT):

PTM = PIN - POUT

77
Q

What is the difference between driving pressure and transmural pressure?

A
78
Q

When isolated from the other structures, do the lungs always want collapse to a lower volume?

A

yes

79
Q

What is transpulmonary pressure?

A

It is a transmural pressure and it is defined as the difference between alveolar pressure and pleural pressure.

80
Q

Do the lungs expand or collapse when transpulmonary pressure is greater than zero? equal to zero?

A

greater than zero = expand

equal to zero = collapse (pneumothorax)

81
Q

How is the functional residual capacity (FRC) determined? How would FRC change with emphysema (decreased lung recoil)? fibrosis (increased lung recoil)?

A

It is a combination of the resting volume of the lungs and the resting volume of the thorax

FCR would increase

FCR would decrease

82
Q

Name the inspiratory and expiratory muscles

A
83
Q

How do inspiratory muscles move the respiratory system away from it’s functional residual capacity (FRC)?

A

inspiratory muscles increase the volume towards the total lung capacity, while expiratory muscle decrease the volume towards the residual volume

84
Q

What nerve innervates the diaphragm?

A

phrenic nerve (C3, C4, C5)

85
Q

What is Boyle’s law? How does it apply to inspiration?

A

As volume increases, pressure decreases. Therefore, as the diaphragm contracts and increases the volume of the alveolus, the alveolar pressure decreases below atmospheric pressure allowing for air to flow into the lungs

86
Q

Contrast the mechanism for airflow on inhalation during positive pressure breathing with spontaneous breathing.

A

positive pressure breathing = mechanical breathing

spontaneous breathing = breathing on your own

Positive pressure breathing (mechanical ventilation) inflates the lungs by increasing intra-alveolar pressure, rather than decreasing the pressure of the chest wall

87
Q

Contrast the mechanism by which airflow occurs during exhalation and how this process changes with forced exhalation.

A

Exhalation is an almost entirely passive process; once the lung is inflated beyond the resting volume, the elastic recoil of the lungs brings the lungs back to resting volume

Muscular work (using internal intercostals, rectus abdomini, obliques, and transversus abdominis) is required for rapid exhalation, or exhalation beyond the functional residual capacity

88
Q

What is compliance? How is it calculated?

A

Pulmonary compliance (or lung compliance) is a measure of the lung’s ability to stretch and expand

Compliance is analogous to stiffness; a compliant balloon is easy to blow up (requires little transmural pressure to increase its volume)

Compliance = Δ Volume / Δ Transmural Pressure

89
Q

What are the factors that affect compliance?

A
  • Lung stiffness
    • Surface tension
      • Surfactant
    • Parenchymal compliance
      • Emphysema (increased compliance)
      • Fibrotic diseases (decreased compliance)
  • chest wall
  • pleural space
  • abdomen
90
Q

How would an increase in compliance affect this graph? A decrease in compliance?

A
91
Q

What is surface tension?

A

Surface Tension: The millions of alveoli that comprise the lung parenchyma are lined by a thin layer of fluid. At any gas-liquid interface, the more tightly spaced molecules in the liquid have a greater attraction to each other than the more widely spaced molecules in the gas, creating a phenomenon known as surface tension

92
Q

What is surfactant?

A

Known formally as dipalmitoylphosphatidyl choline, surfactant is a detergent produced by Type II pneumocytes that greatly reduces alveolar surface tension.

93
Q

How does surfactant decrease surface tension? increase compliance?

A

surfactant molecules are interposed between the liquid molecules, decreasing their intermolecular forces and, as a result, surface tension. This increases compliance and reduces the muscular effort required during inhalation.

94
Q

What is Infant Respiratory Distress Syndrome (IRDS)?

A

babies make surfactant in the third trimester; when they’re born before then, there’s no surfactant so breathing requires a lot of work

95
Q

How does emphysema increase lung compliance?

A

By destroying alveolar septae and the normal architectural relationships of the lung parenchyma, emphysema increases the compliance of the lung tissue. This makes exhalation more difficult!

96
Q

How does fibrosis decrease lung compliance?

A

fibrosis (i.e., scarring) of the lung parenchyma increases the lung recoil. This makes inspiration more difficult

97
Q

How does kyphoscoliosis affect compliance?

A

Kyphoscoliosis results in restricted chest wall movement which decreases compliance

98
Q

How does excess fluid in the space (pleural effusion), pleural-based masses (e.g., mesothelioma) or thickening of the pleural surfaces due to chronic inflammation affect respiratory system compliance?

A

It results in a decrease in compliance

99
Q

How can ascites or late stage pregnancy affect compliance?

A

It limits the descent of the diaphragm on inhalation, thereby limiting respiratory system compliance.

100
Q

What are the 4 factors that determine airway resistance?

A

Viscosity of the substance

Length of the airway

Diameter of the airway

turbulence

101
Q

Diameter of the airway:

How does bronchial muscle contraction affect airway resistance?

A

it increases resistance

102
Q

Diameter of the airway:

How does radial contraction affect airway resistance?

A

As lung volume increases on inhalation, the enlarging alveoli exert more radial traction on the airways, pulling them open to a higher caliber. With exhalation, the opposite happens; as lung volume declines, the tethering effect diminishes and the airway caliber decreases.

103
Q

Diameter of the airway:

how does mucus secretions affect airway resistance?

A

Airway secretions can effectively decreases airway diameter, increasing resistance

104
Q

Diameter of the airway:

How does mucosal and peribronchial edema affect airway resistance?

A

fluid in the interstitial spaces can compress the surrounding airways, decreasing radius and increasing resistance

105
Q

What is Reynolds number?

A

The higher the Reynolds number, the greater the tendency towards turbulent flow.

r = radius of the airway lumen

v = velocity

n = viscosity

d = density

106
Q

How is the driving pressure affected in turbulent conditions?

A

driving pressure is proportional to the square of flow

107
Q

How does pediatric lung mechanics differ from adults?

A
  • Have a more compliant chest wall → lower FRC than adults (chest wall doesn’t pull the lungs open with as much force), so infants have high respiratory rates and don’t exhale fully to FRC
  • Ribs are more horizontal and less able to perform bucket-handle movement → decreased ability to increase thoracic volume on inhalation
  • Diaphragm is less efficient due to having less of a curvature
  • Airway anatomy
    • Airways have a small diameter! And resistance is proportional to r4!
    • This requires generation of a higher pressure difference to maintain air flow
108
Q

How do lung mechanics change with old age?

A
  • Compliance decreases
    • Kyphosis
    • Stiffened thoracic cage from calcification
  • Loss of muscle strength
  • Elastic fibers degenerate (starting at age 50)
    • Increases compliance
    • Reduces tethering effect on airways that typically helps reduce airway resistance at higher lung volumes
    • Can result in premature closing of airways on exhalation → trapping of air and hyperinflation (called senile emphysema)
109
Q

Explain the mechanism behind the development of tolerance to inhaled B2 agonists.

A

GPCR kinases phosphorylate the stimulated B2 receptor → B-arrestins bind to receptor → receptor is inactivated → receptor becomes desensitized → receptor gets endocytosed

110
Q

Describe the classification criteria for the severity of asthma when determining the initial treatment regimen and describe the treatment used for patients in each class.

A

Intermittent disease: 2 day/week or fewer symptoms, 2x/month of fewer nocturnal awakening, >80% FEV1 - give a SABA (albuterol) prn

Persistent disease:

Mild: more than 2 day/week symptoms, 3-4x/month nocturnal awakening, minor activity interference, >80% FEV1 - give low-dose ICS (fluticasone) + SABA (albuterol) prn

Moderate: daily symptoms, more than 1x/week nocturnal awakening, interference w/ activity, 60-80% FEV1 - give moderate-to-high dose ICS (fluticasone) + LABA (salmeterol or formoterol) + SABA (albuterol)

Severe: symptoms many times/day, nightly nocturnal awakening, extreme activity interference, <60% FEV1 - give high-dose ICS (fluticasone) + oral corticosteroid (prednisone) + LABA (salmeterol or formoterol) + SABA (albuterol)

111
Q

What is the data regarding giving a LABA (only a LABA - without any steroids) to patients with asthma?

A

Mortality rates are higher when a LABA alone is given to asthma patients vs. when a corticosteroid is given

112
Q

Describe the criteria for GOLD spirometry staging (stages I - IV) for patients with COPD.

A

Stage I (mild): ≥80% predicted FEV1

Stage II (moderate): 50-79% predicted FEV1

Stage III (severe): 30-49% predicted FEV1

Stage IV (very severe): <30% predicted FEV1

113
Q

Describe how GOLD spirometry staging is used in conjunction with symptom severity to classify COPD patients when determining a treatment plan. Describe the treatment plans for each symptom severity class (A through D).

A

For patients with stage I or II spirometry staging:

Class A (low symptom severity): give inhaled short-acting anti-muscarinic (ipatropium) or a SABA (albuterol)

Class B (high symptom severity): give inhaled long-acting anti-muscarinic (tiotropium) or a LABA (salmeterol or formoterol)

For patients with stage III or IV spirometry staging:

Class C & D (low and high symptom severity - treatments are the same):

Option 1: inhaled corticosteroid (fluticasone) + LABA (salmeterol or formoterol)

Option 2: inhaled long-acting anti-muscarinic (tiotropium)

114
Q

Are anti-muscarinic drugs used for asthma patients?

A

Nope - studies show they don’t really help

115
Q

What treatment strategy is used for patients presenting with exacerbation of COPD?

A

First, exclude other potential causes of the exacerbation (pneumonia, for example).

To calm down the COPD: use aggressive bronchodilators, systemic corticosteroids (prednisone), antibiotics (azithromycin cuz it has anti-inflammatory properties - controversial but there may often be subclinical bacterial infections in these patients)

116
Q

What is the major difference between the first and second-generation anti-histamine drugs?

A

1st generation anti-histamines are lipophilic and cross the blood-brain barrier, so they can be used to treat a wider variety of conditions: allergy, motion sickness, anxiety, insomnia.

They also have more side effects: dry mouth, urinary retention, flushing, hallucinations, convulsions, tachycardia, coma.

117
Q

What is the criteria for having demonstrated a positive bronchodilator response during spirometry testing?

A

200mL and 12% increase in either FEV1 or FVC after drug administration

118
Q

Your 63 yo patient presents with shortness-of-breath and demonstrates a .56 FEV1/FVC ratio on spirometry. They have a 30 pack-year smoking history and you notice that they exhale with pursed lips and use accessory muscles during breathing, especially during exhalation. Their lateral CXR looks like this…

What is your Dx?

A

Emphysema. Note flattened diaphragm and increased retrosternal air space.

119
Q

What is the only treatment shown to improve life expectancy in COPD patients other than smoking cessation? When is it indicated?

A

Long-term oxygen therapy. Indicated when patients have a resting PaO2 of 55mmHg or less, or a SpO2 of 88% or less.

120
Q

Where are peripheral chemoreceptors located and what do they respond to?

A

Located in the carotid and aortic bodies, they respond mainly to hypoxemia (low PaO2), but also sense pH.

121
Q

Where are central chemoreceptors located and what do they respond to?

A

In the brainstem - the ventrolateral surface of the medulla. Respond mainly to pH changes in the CSF from CO2 (CO2 crosses the BBB easily)

122
Q

How do PaO2 levels alter changes in ventilation as PaCO2 levels increase?

A

At low PaO2 levels, the response to increasing PaCO2 levels is increased (higher sensitivity) - see graph

123
Q

Define obesity hypoventilation syndrome.

A

Obesity hypoventilation syndrome is defined as daytime hypercapnia (PaCO2 > 45 mmHg) in an obese person (BMI over 30)

124
Q

Should you do pulmonary function tests for evaluation of acute dyspnea?

A

Hellz nah, only for chronic dyspnea.

125
Q

Fill in the 6 blanks.

A
  1. IRV - inspiratory reserve volume
  2. FRC - functional reserve capacity
  3. ERV - expiratory reserve volume
  4. VC - vital capacity
  5. TLC - total lung capacity
  6. RV - residual volume
126
Q

Describe the cut-offs for normal vs. abnormal for the following PFTs: FEV1, FVC, TLC, RV, DLCO, FEV1/VC

A

FEV1, FVC, and DLCO: <80% predicted value is abnormal

TLC and RV: between 80-120% predicted value is normal

FEV1/VC: below 0.7 is abnormal (obstructed)

127
Q

What is this flow-volume loop suggestive of?

A

Obstructive disease

128
Q

What is this flow-volume loop suggestive of?

A

Restrictive disease

129
Q

What is this flow-volume loop suggestive of?

A

Variable intrathoracic obstruction

130
Q

What is this flow-volume loop suggestive of?

A

Variable extrathoracic obstruction

131
Q

What is this flow-volume loop suggestive of?

A

Fixed obstruction

132
Q

What pulmonary function test result is the hallmark of restrictive lung disease?

A

Low TLC

CPR (27 decks)

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